Explore the Potential with AI-Driven Innovation
The specialised, focused library is developed on demand with the most recent virtual screening and parameter assessment technology, guided by the Receptor.AI drug discovery platform. This approach exceeds the capabilities of traditional methods and offers compounds with higher activity, selectivity, and safety.
The compounds are cherry-picked from the vast virtual chemical space of over 60B molecules. The synthesis and delivery of compounds is facilitated by our partner Reaxense.
In the library, a selection of top modulators is provided, each marked with 38 ADME-Tox and 32 parameters related to physicochemical properties and drug-likeness. Also, every compound comes with its best docking poses, affinity scores, and activity scores, providing a comprehensive overview.
We employ our advanced, specialised process to create targeted libraries.
Fig. 1. The sreening workflow of Receptor.AI
Our methodology employs molecular simulations to explore a wide array of proteins, capturing their dynamic states both individually and within complexes. Through ensemble virtual screening, we address conformational mobility, uncovering binding sites within functional regions and remote allosteric locations. This thorough exploration ensures no potential mechanism of action is overlooked, aiming to discover novel therapeutic targets and lead compounds across an extensive spectrum of biological functions.
Several key aspects differentiate our library:
partner
Reaxense
upacc
Q8IXM3
UPID:
RM41_HUMAN
Alternative names:
39S ribosomal protein L41, mitochondrial; Bcl-2-interacting mitochondrial ribosomal protein L41; Cell proliferation-inducing gene 3 protein; MRP-L27 homolog
Alternative UPACC:
Q8IXM3; Q96Q49
Background:
Large ribosomal subunit protein mL41, also known as 39S ribosomal protein L41, mitochondrial, plays a crucial role in the mitochondrial ribosome's large subunit. It is pivotal in apoptosis and cell cycle regulation, enhancing p53/TP53 stability and its mitochondrial translocation, thereby promoting p53/TP53-induced apoptosis under growth-inhibitory conditions. It also arrests the cell cycle at the G1 phase by stabilizing CDKN1A and CDKN1B proteins.
Therapeutic significance:
Understanding the role of Large ribosomal subunit protein mL41 could open doors to potential therapeutic strategies.